T
Tsung Cheng Chang
Researcher at University of Texas Southwestern Medical Center
Publications - 40
Citations - 18898
Tsung Cheng Chang is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: microRNA & Gene silencing. The author has an hindex of 22, co-authored 35 publications receiving 15021 citations. Previous affiliations of Tsung Cheng Chang include Johns Hopkins University & University of Texas Health Science Center at Houston.
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Journal ArticleDOI
StringTie enables improved reconstruction of a transcriptome from RNA-seq reads
Mihaela Pertea,Geo Pertea,Corina Antonescu,Tsung Cheng Chang,Joshua T. Mendell,Steven L. Salzberg +5 more
TL;DR: StringTie, a computational method that applies a network flow algorithm originally developed in optimization theory, together with optional de novo assembly, to assemble these complex data sets into transcripts produces more complete and accurate reconstructions of genes and better estimates of expression levels.
Journal ArticleDOI
Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis
Tsung Cheng Chang,Erik A. Wentzel,Oliver A. Kent,Kalyani Ramachandran,Michael Mullendore,Kwang Hyuck Lee,Georg Feldmann,Munekazu Yamakuchi,Marcella Ferlito,Charles J. Lowenstein,Dan E. Arking,Michael A. Beer,Anirban Maitra,Joshua T. Mendell +13 more
TL;DR: It is demonstrated that microRNAs (miRNAs) are important components of the p53 transcriptional network and miR-34a-responsive genes are highly enriched for those that regulate cell-cycle progression, apoptosis, DNA repair, and angiogenesis.
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c-Myc suppression of miR-23a/b enhances mitochondrial glutaminase expression and glutamine metabolism.
Ping Gao,Irina Tchernyshyov,Tsung Cheng Chang,Yun-Sil Lee,Kayoko Kita,Takafumi Ochi,Karen I. Zeller,Angelo M. De Marzo,Jennifer E. Van Eyk,Joshua T. Mendell,Chi V. Dang +10 more
TL;DR: In this paper, the c-Myc (hereafter referred to as Myc) oncogenic transcription factor, which is known to regulate microRNAs and stimulate cell proliferation, transcriptionally represses miR-23a and miR23b, resulting in greater expression of their target protein, mitochondrial glutaminase, in human P-493 B lymphoma cells and PC3 prostate cancer cells.
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Therapeutic microRNA Delivery Suppresses Tumorigenesis in a Murine Liver Cancer Model
Janaiah Kota,Raghu R. Chivukula,Kathryn A. O'Donnell,Erik A. Wentzel,Chrystal L. Montgomery,Hun-Way Hwang,Tsung Cheng Chang,Perumal Vivekanandan,Michael Torbenson,K. Reed Clark,K. Reed Clark,Jerry R. Mendell,Jerry R. Mendell,Joshua T. Mendell +13 more
TL;DR: It is demonstrated that hepatocellular carcinoma (HCC) cells exhibit reduced expression of miR-26a, a miRNA that is normally expressed at high levels in diverse tissues that may provide a general strategy for miRNA replacement therapies.
Journal ArticleDOI
Widespread microRNA repression by Myc contributes to tumorigenesis.
Tsung Cheng Chang,Duonan Yu,Yun-Sil Lee,Erik A. Wentzel,Dan E. Arking,Kristin M. West,Chi V. Dang,Andrei Thomas-Tikhonenko,Joshua T. Mendell +8 more
TL;DR: In this paper, the c-Myc oncogenic transcription factor (Myc) is pathologically activated in many human malignancies and the predominant consequence of activation of Myc is widespread repression of miRNA expression.